Modulation of Ischemic Neuronal Death by Non-lethal Ischemia and Ubiquitin Reappearance in Gerbils

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Tolerance to lethal ischemia can be induced in gerbils by prior subjection to non-lethal ischemia. The sequential changes og ubiquitin immunoreactivity in the hippocampi of gerbils subjected to non-lethal ischemia followed by lethal ischemia were investigated. The double-ischemic group was subjected to non-lethal ischemia followed by lehtal ischeima, the single-ischemic group was subjected to lethal ischemia, only, the sham-ischemic qroup was subjected to sham operation followed by lethal ischemia. The densities of the CA (Cornu ammonis) 1 neurons were assessed by hematoxylin-eosin staining. In the double-ischemic group, the extent of the neuronal damage was less than that in the single-ischemic and sham ischemic groups (both P<0.02) and half that in the control group (P<0.002). Ubiquitin immunoreactivity (UIR) disappeared once after lethal ischemia in all the ischemic group (P<0.002). Ubiquitin immunoreactivity (UIR) disappeared once after lethal ischemia in all the ischemic groups. In the single and sham ischemic groups, UIR never reappeared, whereas in the double-ischemic group, it recovered partially during the early postischemic period and almost completely in the surviving cells eventually. Non-lethal ischemia reduces the ischemic damage caused by subsequent lethal ischemia in the Cai neurons of gerbils, and ubiquitination is related to the damage reduction.
Yamaguchi University Graduate School of Medicineの論文